I usually enjoy Dr. Roberts' literature reviews but I'm going to poke a little bit of fun here. Osler died in 1919, not a guy known for his skills at resuscitating cardiac arrest as CPR really didn't even come around until the 1960s. He is now best known for his appearances on powerpoint slides.

His recommendations for treating arrhythmia are actually pretty fun to read though:

"...at least ten hours of the 24 should be spent in the recumbent posture. A tepid bath may be taken in the morning, or, if the patient is weakly and nervous, in the evening followed by a vigorous rubbing... articles of food known to cause flatulency should be avoided. Sexual excitement is particularly pernicious, and the patient should be warned specially on this point."

Sir William Osler. The principles and practice of medicine. 1909. Googlebooks (free).

July 1, 2011

Do you remember that table from the back of First Aid for Step One? The one with about 10 pages of word associations? When I say "Auer rods" you say "AML"; when I say "negative birefringence" you say "gout." What an unbelievably stupid way to learn, and shame on the NBME for encouraging this style.

Yet much of clinical practice is based on just such things, little free associations. These associations are often passed on as teaching points on shift and I understand why - they are digestible and quick. This kind of stuff, however, reinforces the very worst kind of medical knowledge acquisition - isolated facts devoid of clinical relevance and sometimes incorrect.

Although the statue is made of stone, his heart is made of chocolate.Hannibal, Sebastien Slodtz (marble) 1655: Louvre, Paris

When I say "digoxin toxicity," you say "stone heart." It's a classic free association; but is it true?

Many of us have probably heard some rumblings that this might not be all that big of a deal. I just came off Toxicology at Toxikon in Chicago. One of the other residents on with me, David Schrift from the UIC EM/IM combined program, gave a great 30 minute talk on this topic. David went through all the literature and I was not surprised to find that it was incredibly weak. Some of the research actually required him to go to the library and get photocopies!

Disclaimer: this is not original MDA work; David produced all of this stuff and graciously agreed to let me reproduce it.

The initial incident that started this nonsense about Calcium + Dig being dangerous was a paper from The JAMA in 1936. There were 2 case reports and then a weird little experiment.

Case #1: 32F s/p cholecystectomy for acute cholecystitis hypotensive and tachy on POD #2, given digalen for PVCs, medicine consult recommended IV calcium for “toxic irritation of the accelerator mechanism through sympathetic involvement." She got some calcium, seized and died.

Case #2: 55M with hypercalcemia (MM? hyperparathyroid?) presented with bilateral femur fractures. To OR for hemithyroidectomy where he got digalen, developed post-op tetany, got a 1g CaCl bolus, and died.

As David pointed out, in neither case were the electrolytes, acid base status, dig level, or infusion rate of calcium noted. In both cases there were clear other reasons for death. Plus, what the heck is "toxic irritation of the accelerator mechanism" and why would it be treated with IV calcium? This was followed up be a small experiment where dogs were given dig+calcium and some died. Again, many details were omitted. So a body of literature developed over the following decades, but it wasn't good literature.

David did a really cool thing and took all the studies (many of which were animal) and converted the Calcium infusion rates to the equivalent of grams of calcium gluconate given to a 70 kg adult. The results will surprise you. I have modified his table slightly:

Giving Calcium to dig toxic patients is almost certainly ok. The body of literature that says it isn't is not relevant to our practice. In the Archives of Internal Medicine paper, the dogs were getting up to496g CaGlu equivalents at 15-147 g/min. Even Seth doesn't do that.*

In the American Heart Journal paper, the dogs were loaded with 2.4-5 g/min of calcium and then given digitalis until the went into VTach. Again, we don't do that.

The 2004 Journal of Toxicology study took 12 pigs and loaded then with digoxin; all were noted to have hyperkalemic ECG changes. They got 2g CaClu or saline. There was no change in time of death. This was a small study to be sure, but seems more relevant than bombing some poor dog with IV calcium.

That said, calcium will not be life saving in true dig toxicity. As the tox fellow pointed out during David's talk, if a patient is truly dig toxic, they need DigiBind. This information is only helpful for the ill patient who presents with a wide complex ECG, renal failure, and hyperkalemia** who is on dig but for whom the dig level is not yet known.

Give the calcium, but don't do it at 147 g/min.

-MJP

from seth:Debunking pseudoaxioms is fun.*I routinely give my patients 496g at 147g/min and anyone who doesn't is committing malpractice**,*****This is not medical advice.***This is not legal advice, nor is it my practice.

June 19, 2011

In an essay in Vanity Fair in December 2001 the incomparable Christopher Hitchens described wandering through the charred and broken remains of lower Manhattan. He reflected on New York as the center of the world; a place of multiculturalism and openness that was horribly assaulted by nihilists and psychopaths. I'll never forget what he said:

One has to be capable of knowing when something is worth fighting for. One has to be capable of knowing an enemy when one sees one.

As much as we like primary literature, every so often you have to remind yourself that disease is the enemy, and like the enemy Hitchens recognized in the assailants of New York, disease is worth fighting. Aleksander Hemon's haunting piece The Aquarium in this week's New Yorker is the best account of a family struggling with disease I have read in years, possibly ever. His infant daughter is diagnosed with a rare brain tumor and goes on to die in the PICU at Children's Memorial Hospital in Chicago (where I work). Along the way she is subjected to multiple chemo regimens:

His description of his daughter's cardiac arrest and death is almost unreadable unless you give yourself a break in the middle. Finally, after she is gone, Hemon reflects on her death and suffering in a way that I think we would do well to remember:

One of the most despicable religious fallacies is that suffering is ennobling --that it is a step on the path to some kind of enlightenment or salvation. Isabel's suffering and death did nothing for her, or us, or the world. We learned no lessons worth learning; we acquired no experience that could benefit anyone. And Isabel most certainly did not earn ascension to a better place, as there was no better place for her than at home with her family. Without Isabel, [my wife] and I were left with oceans of love we could no longer dispense; we found ourselves with excesses of time that we used to devote to her; we had to live in a void that could be filled only be Isabel. Her indelible absence is now an organ in our bodies, whose sole function is continuous secretion of sorrow.

May 28, 2011

My dislike for PE works on many levels. On the one hand, PE can be fatal, and I generally don't like it when my patients die. On the other hand, many or even most PE (or is it PEs? or PE's?*) aren't particularly dangerous.

Further, we don't really know the prevalence of PE, we don't know how to tell dangerous PE from not-particularly-dangerous PE, and we're not even sure about the treatment for PE.

As discussed at length in what I think is still the best episode to date of SMART-EM, the evidence is not only weak but maybe even suggests that perhaps we shouldn't anticoagulate patients with PE at all, despite the clear "standard of care." And while thrombolysis might benefit some very sick patients with PE, nobody really knows.

Further, some very smart people suggest that a main function of the lungs might be to filter clots from making it to the brain.

That's not to say that PE isn't a dangerous entity. A new study by Weiner et al in the Archives of Internal Medicine notes that introduction and widespread adoption of CT pulmonary angiography has increased the diagnosis of PE about 70% but decreased the case fatality rate by only half that much, and overall mortality only modestly decreased. To be honest, I'm not completely clear on whether "case fatality rate" means much; they define it as "the proportion of hospital deaths among patients with a PE."

Not surprisingly, the rate of what appear to be clinically important complications of anticoagulation also increased by about 70%.

This is certainly not a perfect study. The study authors use mortality from death certificates as the primary outcome measure, and as someone put it, cause of death is largely determined by interns.

As the study authors discuss, the increase in PE diagnosis could be a good thing if more diagnosis means better outcomes. However, in the absence of better outcomes, we are likely diagnosing clinically insignificant disease. And there's no way to determine if the PE I just diagnosed is one of the bad ones or not.

So we use a lot more CTPA (not news) to detect a whole lot more PE, with minimal benefit. And I don't think the "ease" of CTPA is the only part of it. The Wells Criteria, d-dimer, and PERC were supposed to help us safely decrease testing, but aren't used properly, have lead to increased testing, and may not even work. Specifically, many physicians seem to use the d-dimer to increase, not decrease, testing. Despite our best intentions, perhaps the overall increase in conversation about PE leads to increased testing on it's own (i.e., availability bias).

Moreover, it's not just about diagnosing more patients with PE or deciding who to anticoagulate. It's not even about the very real radiation risks. As crowding becomes the norm in many EDs, many departments operate at full capacity much of the time. At both of the hospitals where I work, the CT scanners run non-stop. So each extra CT means that other patients have to wait for their own CT scans, each of them requiring nursing care, physician attention, and all of the other trappings of being in the department. In the age of ED crowding, everything has an opportunity costs. Crowding leads to overworked nurses, frustrated physicians, and all sorts of bad outcomes, including worse pain management; delays to antibiotics, thrombolytics and PCI; missing quality measures; increased mortality; and decreased patient satisfaction. If an extra CT means 12 patients wait for an extra half hour (my estimate) that means 6 more patient-in-ED-hours, with a conservative estimate of 2% increased mortality for every 6 extra hours patients spend in the ED. Does that mean every 50 extra CTs could mean that 1 more patient dies from crowding?**

I'm not sure what to do with all of this. Concern about PE seems genuine. (Boehringer Ingelheim developed dabigatran for primary stroke prevention in afib, not to treat PE. Compare about 500 cases per 100,000 vs. 112 cases per 100,000.) PE can be fatal. CTPA can detect PE. Initiating treatment may save a patient's life, but anticoagulation probably has limited benefits and carries very real risks. There don't seem to be easy answers.

But some things are clear:
We irradiate far too many people, and some people are destined to a life of eating rat poison.

*I think it's either PE or PEs, but not PE's.
**This is admittedly a very rough, back-of-the-envelope estimate that I made up. Perhaps in the future it can be quantified more accurately.
UPDATE 7/21/2012:
2 interesting recent articles:

May 24, 2011

We've been talking lately about resident conference attendance at my shop. It has always seemed to me that sitting a bunch of adults down and reading slides to them is an incredibly poor way to have them learn anything.

As a thought experiment: try to remember even a conference TOPIC from your lecture series last month. Bet you can't.

For what it's worth, I spent most of my second year of medical school snoozing the back of the lecture hall or doing crossword puzzles with Harold Bach. I studied, but lecture bored me nearly to death.

Since we're all a bunch of nerds (especially Seth) we looked up some data. Hern et al. showed that attendance at conference is poorly correlated with scores on the EM inservice exam. Michelle Lin has a much better discussion of this than I could ever manage over at ALIEM.

Mostly in conference I fiddle with my Blackberry and fantasize about switching to the Droid X. It is so silly to walk off a busy shift with critical patients to go listen to someone read PPT slides about pediatric abdominal pain; I wish the RRC would realize this and half conference time.

The last conference I gave was Weingart inspired: I talked about my practice (a little bit presumptuous for a PGY3) with vascular access and said some controversial things such as:

femoral lines suck (actually this is just true)

peripheral dopamine sucks

you can do subclavians in patients with mild to moderate coagulopathy without worrying too much

arterial lines can be quite dirty

Not everyone agreed with me, but we spent most of the time arguing back and forth. I didn't see anyone snoozing. I also used Prezi, which you should check out, instead of powerpoint.

When I am king* I will ban the following:

epidemiology slides

progressive maps showing how fat/diabetic/hypertensive/old the US population is getting

pathophysiology slides that take up more than 0.04% of the total talk

attempts to make boring lectures clinically relevant by having mini-cases

lectures about basic life skills, e.g. how to talk with people on the phone

-MJP

*Seth will be court jester, housing czar, Defense Minister, and ambassador to Laos.

from seth:

To combat conference atrophy, we're implemented an Asynchronous Learning curriculum, where residents will review book chapters, podcast episodes, or other resources, summarize them online, and create a quiz. Residents can get credit by either posting their own content or taking others' quizzes. Not a huge step but the goal is to encourage and reward the use of some of the great educational resources out there, while cutting down on didactic time, theoretically leaving the remaining traditional conference higher-yield (Grand Rounds, resident M&Ms, our new-and-improved journal clubs, and trauma/critical care talks).

May 7, 2011

Let me start out by saying that this is a shameless plug for one of my own research projects. Actually, the real credit for this study goes to Erin Quattromani, one of my co-residents, and Emilie Powell, a fellow at my program.

Basically we looked at a national inpatient sample of adults admitted for pneumonia. Erin and Emilie (with help from several others attendings) stratified hospitals according to their performance on the Center for Medicare Studies quality measure for getting appropriate antibiotics in pneumonia patients within 6 hours.

Unsurprisingly for those familiar with the controversy surrounding this quality measure, we didn't find much difference in mortality.

Now there are plenty of limitations and you could pick about the methodology until you were blue in the face. All we really said was:

Hospitals that are the best at getting antibiotics within 6 hours are not hospitals with the lowest inpatient mortality.

Again, pick apart to your heart's content.

That said, I did some of the lit search into how this rule came up and found that its scientific basis is shaky at best. For the best breakdown of this, see the Yu and Wyer paper I cite at the bottom.

Basically there were these two big studies of old, sick Medicare patients publishes in The JAMA and in Archives of Internal Medicine. They showed a trend towards increased survival with early antibiotics.

So there you go: because in 2004 someone showed that 84 year olds with cancer and pneumonia do better with early antibiotics, hospitals get dinged when you don't get them into your otherwise healthy 45 year old male on time.

The truly shocking thing is that there is decent research to suggest that attempted compliance with this silly rule has led to diagnostic errors, overtesting, and (worst of all) administration of antibiotics to patients who didn't need them.

Don't just do something-- stand there (at least until you know the damned diagnosis!).

-MJP

seth says:One of the key differences between the data that suggest early antibiotics may be good and the CMS rule is that the studies were done with ED diagnoses of pneumonia, whereas CMS dings hospitals for missing the 4 hour window on patients with a discharge diagnosis of pneumonia. I can speculate that the patients who are not diagnosed initially with pneumonia may have more complex presentations and therefore might be sicker and more likely to die, but the truth is that no one knows.Also, the PORT scoring system (or Pneumonia Severity Index) is a great tool to estimate mortality associated with pneumonia, but a lot of studies (and clinicians) use it as an admission criterion, although it has not been prospectively validated as a disposition tool.-nst

It's not news that urine tox screens are useless; that's what I've been taught since medical school (admittedly, not all that long ago).

Emergency textbooks such as Tintinalli's (I checked) and PEER VII, the major board review for EM residents, agree. To me, the issue seems pretty much settled.

However, the people we admit our patients to -- internists and psychiatrists -- (anecdotally) always ask for the tox screen. The seemingly compelling argument from psychiatrists is that knowing what drugs were abused now helps with long-term care, i.e. they can catch their patients lying about drug abuse.* Internists seem to be genuinely interested in finding the cause of the patient's current illness, so that other causes can be lowered in the differential.

Although these goals are laudable, unfortunately, as the key table below from the Brahm paper highlights, tox screens are terrible tests. Not surprisingly, most labs put disclaimers in the their u-tox results, such as:

This assay provides a preliminary qualitative analytical test result. A more specific alternate chemical method must be used to obtain a confirmed analytical result, and should be correlated with clinical findings.

My general practice has been to order the urine tox to placate the inpatient teams as I don't want to start fights all the time, but I clarify with the nurses that obtaining a urine sample is their lowest priority.

The point here isn't that tox screens or internists are useless, merely that we should know how good our tests are when we decide whether or not to use them. Routine "screening"** labs are no different.

Unfortunately, my department recently came to an agreement with our Internal Medicine department about standard labs resulting before patients are listed for admission. The general idea is that there are a few levels of care -- a nurse practitioner/hospitalist floor service, a teaching/resident floor service, a handful of stepdown beds, and the ICU. Some patients are too sick for a the NP/hospitalist service and routine labs may identify a subset of those.

But a large group of patients are clearly sick enough for the teaching service but obviously not sick enough to need to be upgraded to a stepdown or unit bed -- and routine labs are not going to identify any patients that might be. An INR of 7 or a surprising new renal failure does not mandate a stepdown bed. Yet these patients now, by interdepartmental policy, cannot be listed for admission until their routine labs result, regardless of the fact that those results will not alter the patients' disposition. This means that patients wait for generally at least an extra hour before they can be admitted, leading to further ED boarding, which leads to, among other things, higher mortality. This is another unfortunate example of misapplied testing leading to worse patient care.

-nst

*This argument was presented by a psychiatry resident at a joint EM-Psych resident conference last year.**The term "screening" for routine labs is broadly misapplied, occasionally by myself. A screening test should be sensitive but not specific to catch all possible instances of disease; routine labs (e.g. chemistry and complete blood count) are incredibly insensitive for disease processes.

April 26, 2011

September 21st, 2010

Traumatic LP for Meningitis

Special thanks to Reuben for inviting me to post this review from my teaching resident rotation.

Question:
Is a “corrected” CSF WBC count accurate for diagnosing meningitis for a traumatic LP?
Background:
Traumatic lumbar punctures may obscure accurate diagnoses. Many authors suggest correcting the WBC count by various methods — the most popular seem to be either 700 RBC = 1 WBC, or by using the actual patient’s RBC:WBC ratio in the blood. While this seems intuitive, does it work?Answer:
Probably not.

Basically, no; the calculations are not helpful. Butif the WBC count is MUCH higher than expected, it’s probably a positive tap.

Key points:

The sources I could find simply assert that correction is a viable method; I could not find any actual evidence that these corrections are valid.

Multiple small studies show that corrections are generally not accurate (including ref. 1), with ROC curves equivalent regardless of how — or if! — correction is applied

However, a few small studies also show that bacterial meningitis may be obvious despite a traumatic tap (refs 2 & 3):

If the “observed:predicted” ratio of CSF WBCs is >10, then some authors conclude that it indicates bacterial meningitis. Sensitivity & specificity are both around 80-90% with this method.

This is a predicted ratio of 1000:1 (RBCs are reported as 10^6/mcL and WBCs are 10^3/mcL)

A purely traumatic tap in this patient would be expected to look like this:

CSF
2000 RBC
2 WBC

If the CSF looked like this:
2000 RBC
20 WBC

than it is “likely” to be bacterial meningitis (Observed:Predicted = 10)

Looking at the data, I think we can all agree that this CSF is infected:
2000 RBC
200 WBC
(Observed:Predicted=100)

Here are the results from the Bonadio paper:

Bonadio data

Looking at their raw data, the ratio of 100 looks like a much better diagnostic cutoff, although it is probably best to still treat (i.e. antibiose & admit) pending more accurate tests (i.e. culture) if the picture is less clear.

Here is a ROC curve for their data, which looks pretty good altogether:

April 23, 2011

Paul Krugman's excellent April 21, 2011 column criticizes those who argue that increasing market forces in the healthcare economy will decrease costs, especially since it hasn't:

“Consumer-based” medicine has been a bust everywhere it has been tried. To take the most directly relevant example, Medicare Advantage, which was originally called Medicare + Choice, was supposed to save money; it ended up costing substantially more than traditional Medicare. (PK 4/21/2011)

Similarly, my wife -- who does a substantial amount of healthcare billing at her job -- loves to point out that secondary insurance plans that many Medicare patients have decide what is covered or not covered based on what Medicare covers (at least in the nutrition counseling she bills).* Which raises the question: what is the point of having extra coverage if it doesn't cover anything extra?

(This is slightly different than Medicare Advantage; my point here is that purchasing insurance on the free market sounds nice but doesn't work; main goal of these supplemental policies is to decrease cost sharing on covered services.)

Further, there is clearly something different about "purchasing" healthcare than, say, a new 3D flatscreen HDTV. The choice between spending $12,000 on a new TV or an appendectomy isn't a choice if one of those options involves a pretty good chance of getting septic and dying. I'm not a trained ethicist or anything, but that seems about the moral equivalent of a mugger threatening to stab you in the right lower quadrant if you don't give them $12,000.

Medical care, after all, is an area in which crucial decisions — life and death decisions — must be made. Yet making such decisions intelligently requires a vast amount of specialized knowledge. Furthermore, those decisions often must be made under conditions in which the patient is incapacitated, under severe stress, or needs action immediately, with no time for discussion, let alone comparison shopping. (PK 4/21/2011)

Krugman also fails to mention the middleman costs of privatization of health insurance. Overhead for private insurers is close to 30% -- about equal parts profit, paperwork, and effort spent denying claims. Note that most of that overhead is expressly about NOT providing patients with healthcare. Medicare has an overhead of <3%.

-nst

*Few insurance plans cover nutrition counseling in any substantive way. It's very difficult to get appropriate counseling for a myriad of medical problems -- such as gestational diabetes. But most insurance companies will cover foot amputations.

March 5, 2011

Seth has invited me to be his co-blogger; knowing Seth, I suspect an ulterior motive, but that's another post. As a lifelong contrarian, I thought I would title my first post the exact opposite of the tag line of the blog.

Anyway, I got the invite while I was in Ethiopia-- Addis Ababa to be exact working, at a KoreanHospital here (the pic is of the resus bay). They have a functioning ED, a trauma system, and an ICU. For Africa (as I understand it) it's a very good hospital, indisputably the finest in Ethiopia as shown by the number of VIPs treated here.

That said, it's still (emergency) medicine in the developing world, which means things go sloooooowly. Coming out of a fast-paced urban tertiary ED, it gave me pause to reflect on something that is central to the MD aware mindset: very, very few things in the ED or in medicine in general are so time-critical that seconds count.

What I have seen here is head injured patients with GCS 4 who don't get intubated for 45 minutes and keep breathing; comatose patients who wait an hour for a head CT; hypotensive patients who don't get fluids for 20 minutes and don't die; babies with cap refill ~8 seconds who wait 40 minutes for a fluid and bolus, and so forth. They are things that in the USA we get very excited about and start running around to get stuff done, but in reality most things can wait. As Obama would say, let me be clear: I don't think this system is ideal, but it has given me a good deal of perspective on what is an emergency and what is not.

So since I'm over here moving at the speed of Addis I decided to come up with a list of SECONDS-MATTER EMERGENCIES: things in medicine that cannot under any circumstances wait even 30 seconds. I did not include things that must happen cognitively very fast (i.e. cric) but only those that must be in-progress or done in a matter or a few seconds.

Defibrillation

Control of arterial hemorrhage

Decompression of tension pneumothorax

That’s about it, I think.

-MJP

from seth:

This gets at the main thrust behind the “don’t just do something- stand there” philosophy — don't spin your wheels unnecessarily. Seconds-matter emergencies are great opportunities to really help people; it just saddens me when people (routinely) focus on the wrong things — running around like the patient’s going to die in the next 10 seconds unless we push labetalol on the asymptomatic patient at 180/100; or pushing lasix on the APE patient instead of the NIV mask.

6) I post the following comment (currently awaiting moderation) on Centor's original post:

The idea that ordering a CT saves time versus a detailed H&P underscores the mistaken assumptions made by non-emergency physicians about how we care for our patients. Any emergency physician worth her salt knows understands that obviating a CT scan by adding an extra 20-30 minutes interviewing and examining a patient saves much more time & work than simply ordering a scan.
Patients who wait for CT scans take up much more time and many more resources than those who don't. If we can discharge a patient clinically (maybe because of a low Centor score) than they free up all of those resources (e.g. nursing). This is essentially the same reasons why we love to admit those pesky low-risk chest pain patients BEFORE the first troponin comes back — boarding is bad for our patients.

7) I repost that here, doubling the number of posts at my nascient blog (potentially inflating my stats artificially with a self-referencing link).

We therefore suggest that adolescents and young adults who present with worsening pharyngitis and clinical suggestions of bacteremia need hospitalization and empiric antibiotic therapy with either a penicillin/metronidazole combination or clindamycin. While we cannot prove that this aggressive management will prevent the development of Lemierre syndrome, this approach seems prudent given the potential severity of F. necrophorum infections. (3)

Furthermore, in my anecdotal and biased sample of patients that I review clinic notes or follow up on as inpatients, we lowly emergentologists are not at all alone in our imagophilia.